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Dept of Internal Medicine and Medical Specialities, University of Catania, Catania, Italy.
To the Editor:
We read with great interest the article by Luijk et al. 1 describing the time-course of substantial protective effects after a single dose of inhaled fluticasone propionate (FP) on adenosine-5'-monophosphate (AMP)-induced bronchoconstriction in asthma. No change was observed in terms of exhaled nitric oxide (eNO) levels.
These findings would further support the current opinion that airway responsiveness to AMP is more sensitive than eNO, together with other noninvasive markers of airway inflammation, in assessing the response to anti-inflammatory treatments 2, 3. To this end, it must be emphasised that inhaled glucocorticosteroids (GCS) have been shown to increase the provocative concentration causing a 20% fall in forced expiratory volume in one second (PC20) threshold of AMP in a dose-dependent manner, whereas the dose response for eNO, together with many other inflammatory markers, and measures of lung function have all been shown to exhibit a plateau effect at lower doses 4. Thus, the changes observed with eNO are not truly dose dependent, whereas the degree of anti-inflammatory effects of AMP challenge are directly proportional to the dose of inhaled GCS. The idea that AMP bronchial provocation seems to offer substantial advantages over eNO has been recently supported by the work of Prieto et al. 5, in which airway responsiveness to inhaled AMP is a useful predictor for safe dose reduction of inhaled GCS in patients with asthma.
Whereas the previously mentioned studies appear to provide enough information to support an important role for AMP provocation in the clinical setting, the study by Luijk et al. 1 raises some important concerns.
Although the rapid protective effect by a single dose of inhaled GCS has never been studied in asthmatic subjects receiving chronic treatment with GCS, the extreme sensitivity of AMP to these drugs could be detrimental to its potential clinical applications, where it is crucial to assess the dose requirement of topical GCS in asthma management. This is not a trivial issue, since the acute effect on AMP challenge is not specific to FP, but it also appears to be shared with other common inhaled GCS, including beclomethasone and budesonide 6.
Therefore, if we want to investigate adenosine-5'-monophosphate for monitoring inhaled glucocorticosteroid requirements in clinical asthma and establishing the appropriate dose needed to control airway inflammation, patients should refrain from taking steroids for 
24–48 h prior to adenosine monophosphate AMP challenge (as its readout: the provocative concentration of adenosine monophosphate causing a 20% fall in forced expiratory volume in one second could be significantly influenced by the last inhaled dose of glucocorticosteroids).
References
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